To the Editor:
The comments by Georgianos, Balaskas, and Zebekakis are appreciated as they permit clarification of our baseline data of diabetic patients with hypertension. We agree that a single measure of blood pressure or blood glucose defines neither hypertension nor glycemic control. While Georgianos and colleagues are concerned about underestimation of the prevalence of resistant hypertension as a result of lack of blood pressure measurements, Brinker and colleagues,1 Rossignol and associates,2 and Ruzicka and Hiremath3 are equally concerned about overestimation of its prevalence attributable to noncompliance or nonadherence. We are also concerned with overestimation as a result of pseudoresistance.4 Our cross‐sectional study of multidrug antihypertensive therapy was not designed to specifically assess outcomes or prevalence of resistant hypertension. In our judgment, data from a cross‐sectional study listing the total number of antihypertensives and diuretics may be as useful as a 24‐hour ambulatory blood pressure recording on a day when the study patient would be sure to take the full complement of prescribed antihypertensives/diuretics in addition to any number of antidiabetes medications, as listed in the Table. We are not aware of any reports in the diabetes/hypertension literature for which follow‐up of measured blood pressure is delineated together with changes in medications over time as renal function deteriorates or improves, but we agree that such an outcome study would be useful.
Table 1.
Antihypertensive Medication Class Use and Renal Function in 10,151 Hypertensive Type 2 Diabetic Patients
| Class | eGFR <30 | eGFR 30–60 | eGFR 60–90 | eGFR >90 | P Value |
|---|---|---|---|---|---|
| No. | 565 | 2230 | 3924 | 3432 | |
| Diuretic | 405 (71.7%) | 1400 (62.8) | 1641 (41.8%) | 892 (26.0%) | <.001 |
| Calcium channel blocker | 281 (49.7) | 818 (36.7) | 949 (24.2) | (548) (16.0) | <.001 |
| β‐Blocker | 413 (73.1) | 1339 (60.0) | 1546 (39.4) | 842 (24.5) | <.001 |
| Angiotensin‐converting enzyme inhibitor | 212 (37.5) | 1236 (50.4) | 2565 (65.4) | 2308 (67.2) | <.001 |
| Angiotensin receptor blocker | 123 (21.8) | 587 (26.3) | 751 (19.1) | 490 (14.3) | <.001 |
| Vasodilator | 73 (12.9) | 58 (2.6) | 26 (0.7) | 11 (0.3) | <.001 |
| Centrally active | 46 (8.1) | 67 (3.0) | 46 (0.2) | 38 (0.1) | <.001 |
| α‐Blockers | 89 (15.8) | 254 (11.4) | 306 (7.8) | 131 (3.8) | <.001 |
| Nitrates | 84 (14.9) | 192 (8.6) | 127 (3.2) | 32 (0.9) | <.001 |
| Direct renin inhibitor | 8 (1.4) | 3 (0.1) | 7 (0.2) | 3 (0.1) | <.001 |
Abbreviation: eGFR, estimated glomerular filtration rate.
Our cohort demonstrates the usual switch from thiazide to loop diuretics (and potentiation of loop diuretics by thiazides) as renal function decreases, and expected medication changes to avoid hyperkalemia. As requested, we have added a table to demonstrate the antihypertensive medication class use as it relates to estimated glomerular filtration rate (Table).
We found equally interesting the fact that medications used for treating glycemia changed along with estimated glomerular filtration rate. This observation (currently awaiting publication) confirms a similar observation we previously reported in an international trial in a population with moderately severe renal dysfunction.5 Insulin resistance represents a nexus between obesity, type 2 diabetes, renal disease, and hypertension and may be a potential metabolic target for control of each as seen in dramatic changes resulting from bariatric surgery.6, 7
[Correction added on October 27, 2016, after first online publication: The title of the article was corrected from “Treating Hypertension in Diabetic Patients With Advanced Chronic Kidney Disease: What Should We Have in Mind?” to “Response to Panagiotis.”]
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